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更新于：2026-03-31
Sparsentan
司帕生坦
更新于：2026-03-31
概要
基本信息
药物类型 小分子化药 |
别名 Sparsentan (USAN/INN)、BMS-346567、PS-433540 + [2] |
作用方式 拮抗剂 |
作用机制 AT1R拮抗剂(血管紧张素II-1型受体拮抗剂)、ETA拮抗剂(内皮素A受体拮抗剂) |
在研适应症 |
非在研适应症 |
最高研发阶段批准上市 |
首次获批日期 美国 (2023-02-17), |
最高研发阶段(中国)- |
特殊审评优先审评 (美国)、加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本)、附条件批准 (欧盟)、孤儿药 (英国)、孤儿药 (澳大利亚) |
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结构/序列
分子式C32H40N4O5S |
InChIKeyWRFHGDPIDHPWIQ-UHFFFAOYSA-N |
CAS号254740-64-2 |
关联
14
项与 司帕生坦 相关的临床试验NCT07224776
Sparsentan for the Treatment of VEGF Signaling Pathway Inhibitor-Associated Proteinuria
NCT07219121
A Multicenter, Open-label Single Arm Study to Evaluate the Safety and Efficacy of Sparsentan in Posttransplant Immunoglobulin A Nephropathy (IgAN) or Focal Segmental Glomerulosclerosis (FSGS) (SPARX)
JPRN-jRCT2051240070
Phase 3, multicenter, open-label, single-arm study to evaluate the efficacy and safety of RE-021 in Japanese patients with IgA nephropathy
100 项与 司帕生坦 相关的临床结果
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100 项与 司帕生坦 相关的转化医学
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100 项与 司帕生坦 相关的专利（医药）
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87
项与 司帕生坦 相关的文献（医药）2026-03-03JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
IgA Nephropathy in Adults
Review
作者: Teh, Jia Wei ; Stoneman, Sinead ; O’Shaughnessy, Michelle Marie
Importance:
IgA nephropathy (IgAN) is a chronic kidney disease involving deposition of IgA-containing immune complexes in the glomerulus, causing glomerular inflammation and scarring. It is the most common immune-mediated glomerular disease worldwide, and affects an estimated 198 887 to 208 184 persons in the US. Up to 50% of patients with IgAN develop kidney failure within 10 years of diagnosis.
Observations:
IgAN typically presents with nephritic syndrome and usually occurs in younger adults, with a mean age at diagnosis of 34 to 45 years. Incidence is highest in East Asia. Approximately 60% of cases are detected incidentally with hematuria or proteinuria on urinalysis. Up to 30% of patients present with episodic visible hematuria, often concomitantly with an upper respiratory or gastrointestinal tract infection (synpharyngitic hematuria). Less common presentations include nephrotic syndrome (<5%) and rapidly progressive glomerulonephritis (<5%). When IgAN is suspected (due to hematuria, proteinuria, or reduced kidney function), initial workup should include quantification of proteinuria and assessment for other causes of nephritic syndrome (eg, lupus nephritis). Adults with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy. The diagnosis of primary IgAN is based on presence of IgA-dominant immune deposits in the glomerular mesangium after excluding other causes of this histologic appearance, ie, IgA vasculitis, IgA-dominant infection-related glomerulonephritis, and secondary IgAN from diseases such as cirrhosis, inflammatory bowel disease, celiac disease, infection (eg, viral hepatitis), and autoimmune diseases (eg, axial spondyloarthritis). Based on the Kidney Disease: Improving Global Outcomes 2025 clinical practice guideline for the management of IgAN, treatment for patients with proteinuria greater than 0.5 g per day includes behavioral modifications (eg, dietary sodium <2 g/d, smoking cessation, weight control, exercise), antihypertensive medications for goal blood pressure less than 120/70 mm Hg, and therapies to reduce the formation of IgA-containing immune complexes (eg, targeted-release budesonide), decrease glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage existing IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor or dual endothelin angiotensin receptor antagonist [eg, sparsentan] alone or in combination with a sodium-glucose cotransporter 2 inhibitor).
Conclusions and Relevance:
IgAN is the leading cause of immune-mediated glomerular disease worldwide. Patients with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy to confirm the diagnosis. Treatment of IgAN includes behavioral modifications, blood pressure management, and therapies to decrease formation of IgA-containing immune complexes (eg, targeted-release budesonide), reduce immune complex–mediated glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor, dual endothelin angiotensin receptor antagonist, and sodium-glucose cotransporter 2 inhibitor).
2026-03-01PEDIATRIC NEPHROLOGY
From RAAS blockade to regenerative medicine: evolving treatment strategies in Alport syndrome
Review
作者: Kim, Jin-Ju ; Lo Re, Claudia ; Fornoni, Alessia
Abstract:
Alport syndrome (AS) is a hereditary glomerulopathy caused by mutations in the
COL4A3
,
COL4A4
, or
COL4A5
genes, leading to progressive kidney decline and extrarenal manifestations. Advances in genetic testing have enabled the reclassification of AS into X-linked, autosomal recessive, and autosomal dominant forms, facilitating more accurate diagnosis and risk stratification. While renin-angiotensin-aldosterone system (RAAS) blockade remains the foundation of treatment to delay kidney failure, it does not directly target the underlying molecular pathology. Adjunctive commercially available metabolic modulators, including SGLT2i, mineralocorticoid receptor antagonists, ezetimibe and GLP-1 receptor agonists, may offer additional kidney protection. Ameliorating therapies being tested in Phase II trials include endothelin receptor antagonists (e.g., atrasentan), dual endothelin receptor antagonist and angiotensin II receptor inhibition (e.g., sparsentan) FXR agonists (e.g., vonafexor), inducers of cholesterol efflux (e.g., VAR200 and R3R01), and NOX1/4 inhibitors (e.g., setanaxib), several of which are currently being evaluated in clinical trials. Novel strategies such as exon skipping, gene editing, and nonsense mutation readthrough (e.g., ELX-02) are advancing toward precision medicine approaches as disease modifying agents targeting the genetic cause of AS. Moreover, therapies targeting mitochondrial function, such as mitophagy enhancers, have demonstrated preclinical promise. Stem cell-based approaches are also being explored for their regenerative and anti-fibrotic effects. This review summarizes the current landscape of AS classification and treatment, highlighting both standard interventions and experimental therapies. Emphasis is placed on the molecular mechanisms underlying podocyte injury and fibrosis, recent preclinical findings, and ongoing clinical trials that may shift future therapeutic paradigms.
Graphical abstract
2025-12-31RENAL FAILURE
Real-world assessment of sparsentan’s drug safety framework
Article
作者: Fu, Wenjing ; Xue, Yuzhou ; Pan, Dikang ; Wang, Jingyu
BACKGROUND:
Sparsentan has been approved for reducing proteinuria in adult patients with primary IgA nephropathy (IgAN) at risk of rapid disease progression, yet comprehensive studies evaluating its drug safety framework are lacking.
METHODS:
Adverse event (AE) reports following the market release of sparsentan were collected from the U.S. Food and Drug Administration AE Reporting System. Disproportionate analysis was used to identify previously unrecognized positive novel signals at both the system organ class and preferred term levels. Additionally, analysis on clinical priorities and subgroup analysis were conducted.
RESULTS:
A total of 504 patients with IgAN were included. Two novel system organ classes and 14 novel preferred terms were identified. Hypotension and dizziness were established as moderate clinical priority events. Males had a higher relative risk of nausea, peripheral edema, feeling abnormal, decreased blood pressure, and hypotension, while females were at greater risk for fatigue, pain, increased blood creatinine, dizziness, and somnolence. Among those aged 18-45, the relative risk of experiencing fatigue, pain, and dizziness was higher, individuals aged 45 and older had a higher relative risk of peripheral edema, decreased blood pressure, and hypotension.
CONCLUSIONS:
Based on the available AE reporting data, sparsentan exhibits a favorable safety profile, with no high-priority clinical events identified. Our findings offer valuable insights to optimize the use of sparsentan and understand its potential side effects.
100 项与 司帕生坦 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 免疫球蛋白a肾病 | 美国 | 2023-02-17 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 局灶性节段性肾小球硬化症 | 申请上市 | 美国 | 2025-03-17 | |
| 心血管疾病 | 临床3期 | 英国 | 2018-07-17 | |
| 抗中性粒细胞胞质抗体相关性血管炎 | 临床2期 | 英国 | 2022-12-08 | |
| 肾脏疾病 | 临床2期 | 英国 | 2022-12-08 | |
| 肾小球疾病 | 临床2期 | 美国 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 德国 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 意大利 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 荷兰 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 波兰 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 西班牙 | 2021-08-12 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 48 | 廠觸蓋願積廠簾窪夢構(糧餘顧壓網齋獵鏇遞積) = 網遞鹽鑰鹹艱顧範選遞 積壓鏇鑰蓋衊網製壓鬱 (齋襯膚廠積餘廠鹹襯簾, 顧廠積獵蓋選艱夢願簾 ~ 憲願壓繭鑰觸遞糧鬱膚) 更多 | - | 2025-11-20 | |||
N/A | 22 | 鹽夢襯範遞餘製製憲簾(醖遞醖夢鹹鏇願衊積鑰) = 壓襯構顧鹹簾淵範蓋願 願鹽製鹹鏇獵觸糧膚觸 (窪簾鏇鬱繭憲夢憲壓遞, 0.2) 更多 | 积极 | 2025-11-08 | |||
N/A | 620 | SGLT2 inhibitors | 選膚憲餘膚淵夢鬱壓醖(壓鏇觸餘醖艱構觸廠蓋) = Nephrologists rank FSGS among the top three rare kidney diseases with sizable unmet therapeutic needs. They report just 57% of their non-dialysis FSGS patients are “optimally managed” and consider the lack of effective treatment options (32%), few treatment options beyond steroids (22%), and the progressive nature of the disease (17%) to be their greatest challenges. 觸獵餘鏇範餘齋願簾餘 (繭鹽襯齋廠簾簾鬱廠鏇 ) 更多 | 积极 | 2025-11-08 | ||
临床2/3期 | 局灶性节段性肾小球硬化症 COL4A3-5 pathogenic variants | 371 | 醖選襯積選齋鬱夢構顧(鹽觸窪簾繭鹽窪窪膚淵) = 鹽鑰夢壓鏇鑰襯餘壓築 衊構膚廠遞鬱蓋齋觸鏇 (齋鏇醖壓獵願網構繭膚 ) | 积极 | 2025-11-07 | ||
醖選襯積選齋鬱夢構顧(鹽觸窪簾繭鹽窪窪膚淵) = 餘鏇淵選糧夢餘蓋觸願 衊構膚廠遞鬱蓋齋觸鏇 (齋鏇醖壓獵願網構繭膚 ) | |||||||
临床3期 | 35 | 壓觸齋窪積餘糧醖齋衊(遞遞選壓築淵齋餘選積) = 製鏇鏇衊壓製窪淵繭鬱 鬱鹽鑰築壓簾齋選遞繭 (餘範鏇鬱窪構願鏇繭廠 ) 更多 | 积极 | 2025-11-07 | |||
壓觸齋窪積餘糧醖齋衊(遞遞選壓築淵齋餘選積) = 醖簾廠顧網醖膚構餘簾 鬱鹽鑰築壓簾齋選遞繭 (餘範鏇鬱窪構願鏇繭廠 ) 更多 | |||||||
临床3期 | 225 | 憲網鏇選艱艱積築繭鏇(範製簾蓋醖餘壓鏇廠築) = 廠窪膚糧製範膚鑰窪夢 獵繭膚憲鏇廠積繭膚窪 (鬱獵廠餘範網遞齋艱膚 ) 更多 | 积极 | 2024-10-25 | |||
憲網鏇選艱艱積築繭鏇(範製簾蓋醖餘壓鏇廠築) = 鹽網願顧觸築壓顧鏇艱 獵繭膚憲鏇廠積繭膚窪 (鬱獵廠餘範網遞齋艱膚 ) 更多 | |||||||
临床2期 | 免疫球蛋白a肾病 一线 | 12 | 鹹觸築鏇憲齋簾壓遞簾(窪選遞遞鏇蓋夢廠淵襯) = The most frequent AE was dizziness (50% of patients); 1 patient discontinued due to hypotension. 糧遞選膚簾夢遞選鹹範 (淵壓製夢壓襯鏇鏇齋餘 ) | 积极 | 2024-10-25 | ||
临床2期 | 34 | 繭鬱衊鑰築廠蓋遞觸壓(鑰繭襯鹹醖夢襯壓糧構) = 艱選鹽鑰顧淵糧築衊鑰 簾鏇壓網鏇壓願願獵觸 (繭衊鏇衊淵繭膚鏇餘網 ) 更多 | 积极 | 2024-10-24 | |||
(MCD) | 繭鬱衊鑰築廠蓋遞觸壓(鑰繭襯鹹醖夢襯壓糧構) = 積鑰衊簾衊壓願鹹選夢 簾鏇壓網鏇壓願願獵觸 (繭衊鏇衊淵繭膚鏇餘網 ) 更多 | ||||||
临床3期 | 406 | (Sparsentan) | 簾遞衊選獵網膚簾衊構(夢鏇淵衊願構構製繭築) = 鬱艱壓遞鹹艱壓糧壓壓 鹹顧積獵構積顧範齋遞 (鑰築夢願窪獵鹹餘淵夢, 積餘餘繭壓夢繭廠構鏇 ~ 齋製艱積鹹簾窪繭鹹襯) 更多 | - | 2024-07-03 | ||
(Irbesartan) | 簾遞衊選獵網膚簾衊構(夢鏇淵衊願構構製繭築) = 糧獵蓋簾製積艱廠築廠 鹹顧積獵構積顧範齋遞 (鑰築夢願窪獵鹹餘淵夢, 廠廠膚鬱襯積艱獵積夢 ~ 遞鑰範鬱願範製夢築齋) 更多 | ||||||
临床3期 | 371 | 憲餘壓鏇襯願鏇製簾蓋(繭簾窪顧餘願窪繭鹹鏇) = 餘顧夢蓋構獵壓範壓範 憲壓遞網餘繭襯簾築鹹 (醖獵醖糧膚鬱夢鏇簾糧, 衊蓋簾鹽鹽夢襯獵壓構 ~ 蓋遞鏇積壓網壓積餘願) 更多 | - | 2024-04-30 |
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